First Online: 15 July 2009Received: 16 April 2009Accepted: 15 July 2009

Abstract

IntroductionThe dysfunction and decrease of endothelial progenitor cells EPCs may play a very important role in the initiation of organ dysfunction caused by trauma or severe sepsis. We aim to measure the number and function of EPCs in the progression of multiple organ dysfunction syndromes MODS caused by severe sepsis, which may help to understand the pathogenesis of MODS by the changing of EPCs.

MethodsA total of 40 pigs were randomly divided into two groups, which were subjected to hemorrhagic shock, resuscitation and endotoxemia experimental group, n = 20 or acted as a control control group, n = 20. The number and function of EPCs including adhesive, migratory and angiogenesis capacities were analyzed at different times in both groups.

ResultsAll the animals in the experimental group developed MODS 100% and 17 of 20 animals 85% died due to MODS; the incidence of MODS and death of the animals in the control group were 0% P < 0.01. The number, migratory and adhesive capacities of EPCs decreased sharply in the animals of the experimental group corresponding to the increasing severities of MODS, but the angiogenesis function increased gradually until death. The decrease in function of EPCs preceded the decrease in number of EPCs. The decrease in number and function of EPCs occurred prior to the occurrence of MODS.

ConclusionsFor the first time, it was observed that the number and function of EPCs decreased sharply in the progression of MODS and that it was prior to the occurrence of MODS. The decrease in number and function of EPCs may be one of the main pathogenic factors of MODS.